tbuckley/cabot-search huggingface dataset:
Awards,Appointments,Announcements
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Awards,Appointments,Announcements Get access JNCI: Journal of the National Cancer Institute, Volume 83, Issue 19, 2 October 1991, Pages 1376–1377, https://doi.org/10.1093/jnci/83.19.1376 Published: 02 October 1991
Inflammatory bowel disease
Authors: Colms Goggins, Hall O'connell, Weir Dg, Ulcerative Winkelman, W Stenson, The Zileuton
Journal: Gut (1993)

Intercellular adhesion molecule -1 (ICAM-1, CD54) is a cell surface glycoprotein which binds to the LFA-1 (lymphocyte function-activation antigen) on rnononuclear cells and is responsible for important cell to cell interactions within the immune system.Endothelial cell ICAM-1 expression is upregulated by several cytokines eg.TNF, IL-1 beta and IFN-gamma.Increased tissue ICAM-1 expression has been shown in inflammatory disorders, including inflammatory bowel disease.A-circulating-forr-of-ICAM-l (cICAM-1)-has been identified, and elevated serum levels have been found in patients with vasculitis and metastatic malignancies.The aim of this study was to determine the usefulness of serum ICAM-1 levels as an indicator of disease activity in ulcerative colitis.Methods: Serum ICAM-1 levels were measured by ELISA in 23 patients with ulcerative colitis(clinically active; n=i 1 and inactive; n=i 2), and compared levels with serum from healthy controls(n=i 7).Results: There was a significant increase in serum ICAM-1 levels in patients with active versus inactive ulcerative colitis:(31 0.3+/-89ng/ml vs. 204.1+/-46 ng/mI; p=0.003, and in patients with active ulcerative colitis versus controls(310.3+/-89ng/mlvs. 214.3+/-89ng/ml;p=0.01 2).Conclusion: Serum ICAM-1 levels are elevated in patients with active ulcerative colitis and are a useful marker of disease activity.
Fellowships, Grants, Awards
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Fellowships, Grants, Awards Get access JNCI: Journal of the National Cancer Institute, Volume 85, Issue 22, 17 November 1993, Page 1880, https://doi.org/10.1093/jnci/85.22.1880 Published: 17 November 1993
Highlights from Recent Cancer Literature
Journal: Cancer Research (2011)

Glioblastoma Growth after VEGF BlockadeGlioblastoma (GBM) is a highly angiogenic malignancy in which newly formed vessels are thought to arise by sprouting of preexisting brain capillaries in response to increased vascular endothelial growth factor (VEGF) expression/bioavailability.Two recent reports demonstrate that GBM stem cells undergo endothelial differentiation and form a substantial proportion of new vessels in gliomas.These findings describe a new mechanism for tumor vasculogenesis that is not blocked by VEGF inhibitors or VEGFR2 silencing, now a standard of care for patients with progressive GBM.These GBM stem cells were characterized as nestin positive.In a recent article in Cancer Research, di Tomaso and colleagues provide first in-human evidence for nestin expression in GBM and normal brain-associated endothelial cells in GBM patients previously treated with anti-VEGF agents.The authors used autopsy specimens to evaluate vasculature in 5 GBM patients previously treated with the pan-VEGF receptor tyrosine kinase inhibitor cediranib, as compared with 7 other GBM patients who had not received any antiangiogenic agents.Patients who had received cediranib exhibited decreased endothelial cell proliferation and glomeruloid vessels, with vessel diameters and perimeters reduced to levels comparable with those in unaffected contralateral brain hemisphere.In addition, tumor endothelial cells expressed molecular markers specific to the blood-brain barrier, indicative of a lack of revascularization despite the discontinuation of therapy.Surprisingly, in cediranibtreated GBM patients, cellular density in the central area of tumors was lower than in control cases and gradually decreased toward the infiltrating edge, indicative of a change in growth pattern of GBMs after cediranib treatment, unlike that after chemoradiation.Finally, cediranib-treated GBMs showed high levels of platelet-derived growth factor C and c-Met expression, and infiltration by myeloid cells, which may have contributed to anti-VEGF therapy resistance.These findings indicate that GBMs switch their growth pattern after anti-VEGF therapy to enable survival without a second wave of angiogenesis.These insights are timely given recent single-arm phase II results with bevacizumab (anti-VEGF monoclonal antibody) combined with radiotherapy, a strategy that failed to prolong survival in newly diagnosed GBM but was effective at increasing latency of relapse.(Image from cited article's Supplementary Material courtesy of publisher.
Current Medical Literature
Journal: JAMA (1942)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Fellowships, Grants, &amp; Awards
Journal: Environmental Health Perspectives (2006)

Studies submitted under this FOA are expected to identify and characterize the relevant genes, determine their function in normal human reproduction and reproductive development, identify functional partners or pathways and the nature of the interactions, and further our understanding of the consequences of mutations or dysregulation for human reproductive health.Studies of animal models are integral to this effort and are encouraged along with studies involving human subjects.With the completion of the human genome project, the focus of genetic research must shift to functional genomics.NICHD encourages scientists interested in reproduction to lead the way in determining the genes and their mechanisms of action involved in the development of the gonads, reproductive ducts, and genitalia, the processes of gametogenesis, normal and premature reproductive aging, and reproductive disorders such as infertility, cryptorchidism, endometriosis, and polycystic ovarian syndrome (PCOS).Studies on the genetic epidemiology of reproductive disorders might begin with the collection of large numbers of affected patients and their relatives for linkage analysis, association studies or quantitative trait loci (QTL) analysis.Studies using innovative statistical or technical methods are highly encouraged.We also encourage research into epigenetic mechanisms critical to reproduction, especially areas such as the establishment and maintenance of methylation patterns or imprinted loci in the early embryo, the timing, mechanisms, and role of genomic methylation in gametogenesis, the effects of assisted reproductive therapy (ART) on imprinting and genomic methylation, and the reproductive determinants and consequences of X-chromosome inactivation.Reproductive genetics is a broad research area, and the topics discussed and listed below are not meant to be exclusive areas of interest, but rather a sampling of the types of problems that this FOA intends to address.The genetics of sex determination.Sex determination is the translation of the chromosomal sex (XX or XY) into the gender-appropriate internal and external reproductive structures.The initial events of sex determination are, therefore, genetically determined.Errors in the process can range in severity from complete sex reversal to gonadal dysgenesis or minor genital abnormalities.Sex determination, as an early embryological event, can help us address basic questions of the regulation of gene expression, cell-fate determination, and hormone signaling.Approximately one in 1,000 newborns has some abnormality of genital and/or gonadal development.In many cases, gonadal dysgenesis is part of a larger pathologic syndrome, such as Frasier syndrome, Deny-Drash syndrome, or campomelic dysplasia, to name a few.The known genes involved in sex determination often act as growth and/or differentiation factors, and there is mounting evidence that they may be important in tumorigenesis in the gonads as well as other tissues.
Lyme Disease—United States, 1993
Journal: JAMA (1994)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
THE MEDICAL DEPARTMENT OF THE ARMY.
Journal: JAMA (1901)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Editorial board and contents
Authors: Rhiannon Macrae, Milka Kostic, Basil Nyaku, Ria Otten, Patrick Scheffmann, S Gasser, Y Hayashizaki, S Henikoff, H Horvitz, L Hurst, E Koonin, E Meyerowitz, S Moreno, A Nieto, Spain Ponting, J Wysocka, Andreas Wachter, Hamid Bolouri, Katja Taute, Sebastian Gude, Philippe Nghe, Sander Tans, Tatiana Soboleva, Maxim Nekrasov, Daniel Ryan, David Tremethick, Peter Heger, Thomas Wiehe
Journal: Trends in Genetics (2014)
Highlights from Recent Cancer Literature
Journal: Cancer Research (2018)

c-MYC, MYCN, and NeuroblastomaGenomic amplification of MYCN is associated with a poor prognosis in neuroblastoma.Zimmerman and colleagues showed that c-MYC initiated neuroblastoma in transgenic zebrafish, with a shorter latency and higher penetrance than observed with MYCN.Activation of c-MYC in a distinct subset of neuroblastoma tumors occurred either through focal amplification of distal enhancers or enhancer hijacking mediated by chromosomal translocation.The authors suggest that immature sympathoadrenal cells overexpressing c-MYC fail to acquire a terminally differentiated cell identity during embryonal development and instead continue to expand with unregulated growth.Importantly, the clinical outcome for patients with high c-MYC levels was similar to that of patients with MYCN-amplification, a known high-risk driver for this malignancy.Expert Commentary: This work identifies c-MYC as a bona fide oncogene for a distinct group of high-risk childhood neuroblastoma.These data have diagnostic and prognostic importance and may be the basis for future treatment strategies.(Image courtesy of Wikimedia Commons.)
Highlights from Recent Cancer Literature
Journal: Cancer Research (2010)

Resveratrol Suppresses Pancreatic CancerResveratrol (3,5,4 0 -trihydroxy-transstilbene) is a well-known polyphenolic compound of red wine with cancer chemopreventive activity.However, its mechanism of action has not been previously described.Oi and colleagues set out to investigate leukotriene A 4 hydrolase (LTA 4 H) as a target in pancreatic cancer (PDAc).They revealed that knockdown of LTA 4 H in PDAc cells suppressed anchorage-independent growth largely due to limited formation of an LTA 4 H enzymatic product, leukotriene B4 (LTB 4 ).By using an in silico shape-similarity algorithm, the researchers were able to predict that LTA 4 H might be a target of resveratrol.In vitro assays demonstrated that resveratrol directly bound LTA 4 H, and in cell-based models resveratrol suppressed proliferation and anchorage-independent growth of PDAc by inhibiting LTB 4 production and expression of the LTB 4 receptor 1 (BLT 1 ).In vivo, resveratrol inhibited tumor formation in a xenograft mouse model of human PDAc by inhibiting LTA 4 H activity.These findings identify LTA 4 H as a functionally important target for mediating previously undefined anticancer properties of resveratrol.
The Diagnosis of Nervous Diseases.
Journal: JAMA (1952)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Handbuch der pathogenen Mikroorganismen.
Journal: JAMA (1928)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Council on Foods and Nutrition
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Awards, Appointments, Announcements
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Awards, Appointments, Announcements Get access JNCI: Journal of the National Cancer Institute, Volume 81, Issue 20, 18 October 1989, Pages 1537–1538, https://doi.org/10.1093/jnci/81.20.1537 Published: 18 October 1989
Current Medical Literature
Journal: JAMA (1931)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
New and Non official Remedies
Journal: JAMA (1918)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Hypertrophic Cardiomyopathy
Authors: Barry J. Maron, Robert O. Bonow, Richard O. Cannon, Martin B. Leon, Stephen E. Epstein
Journal: New England Journal of Medicine (1987)

(Second of Two Parts)Interrelation between Pathophysiologic Mechanisms and Disease ManifestationsSymptomsThe chief symptoms of hypertrophic cardiomyopathy are exertional angina, dyspnea, fatigue, and impaired consciousness (transient spells of lightheadedness, near-syncope, and syncope). However, a direct, one-to-one correlation between a particular symptom and a single pathophysiologic mechanism does not always exist. For example, in a population of patients with hypertrophic cardiomyopathy, a general relation exists between the severity of symptoms and the magnitude of left ventricular hypertrophy19; however, this correlation is not absolute, and some patients with mild and localized hypertrophy may have severe symptoms,36 whereas other patients with . . .
Editorial Board and Contents
Authors: Paul Craze, Susanne Brink, Paige Shaklee, Jan Kastelein, Ria Otten, Patrick Scheffmann, Göran Arnqvist, Spencer Barrett, Michael Bell, Brendan Bohannan, Ragan Callaway, Stephen Carpenter, James Clark, Paul Dayton, Rodolfo Dirzo, Andrew Dobson, Michael Donoghue, Douglas Irwin, Yoh Iwasa, Stephen Jackson, Christian Köner, William Laurance, Georgina Mace, Robert May, Harold Mooney, Craig Moritz, Randolph Nesse, Isabelle Olivieri, Sarah Otto, Svante Pääbo, Linda Partridge, David Penny, Andrew Read, Daven Presgraves, Benjamin Sheldon, Christine Simon, Boris Worm
Journal: Trends in Ecology & Evolution (2016)
Text Book of Materia Medica for Nurses.
Journal: JAMA (1898)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal